The mechanisms responsible for the production of experimental allergic encephalomyelitis (EAE), a model of autoimmune disease are being examined. Current research is focused on an adoptively transferred model which is produced by the transfer of lymphocytes sensitized against myelin basic protein (MBP) in syngeneic animals. Under optimal conditions, neurological dysfunction occurs; this is characterized pathologically by inflammation and primary demyelination. Many mice recover and develop chronic-relapsing disease. The mechanisms responsible for both the initial and the chronic disease are not known, but an early event is the migration of immune cells across the blood-brain barrier into the central nervous system (CNS). The disease is being studied in strains of mice which differ genetically and vary in the capacity to develop EAE. The investigations are focused on the PL strain, the SJL strain, and Fl progeny. The encephalitogenic epitope for PL mice resides in residues 1-9 of the MBP molecule. Studies are in progress to identify the encephalitogenic epitope in SJL mice. Fl mice are not codominant and develop disease in response to residues 1-9 containing the epitope encephalitogenic for the PL parent. The immune response to MBP and various encephalitogenic peptides are being studied in order to identify the mechanisms responsible for disease in the Fl mice. Antigen presentation by macrophages, capillary endothelial cells in the brain, and astrocytes are being compared. The expression of MHC molecules on these strains is also being evaluated.